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LCRS-Endocrinology > Endocrine Control of Calcium Metabolism > Flashcards

Endocrine Control of Calcium Metabolism Flashcards

1
Q

State some roles of calcium in the body.

A

Control of neuromuscular excitability (hypocalcaemia leads to hyperexcitability because Ca2+ normally blocks the Na+ channels)
Muscle Contraction
Strength in bone
Blood coagulation (Factor IV)- calcium is Factor 4
Intracellular second messenger
Intracellular co-enzyme

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2
Q

Where is calcium mainly stored?

A

Bone - 99% is stored as hydroxyapatite (salt, calcium with phosphorus) crystals in bone

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3
Q

How is calcium present in the blood and what is the concentration of the total calcium ion? What is the main component?

A

-2.5 mM

Unbound ionised calcium (bioactive) - 50%
Bound to plasma proteins - 45% (1.13mM)
Tiny bit as soluble salts (0.13mM)

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4
Q

What is the usual daily intake of calcium?

A

1000 mg/day

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5
Q

What is the concentration of unbound ionised calcium in the blood?

A

1.25 mini Molar (mM), therefore this is the amount that is biologically active component.

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6
Q

What two hormones raise plasma calcium concentration?

A
  • Parathyroid Hormone

- Calcitriol (1,25-dihydroxycholecalciferol) Vitamin D3

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7
Q

What hormone decreases plasma calcium concentration?

A

Calcitonin

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8
Q

Where is parathyroid hormone produced?

A

Parathyroid Glands (four of them) -

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9
Q

Where is calcitonin produced?

A

Parafollicular cells (between follicular cells of the thyroid gland) in the thyroid gland.

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10
Q

Describe the effects of parathyroid hormone on the kidneys.

A

Increases calcium reabsorption

Increases phosphate excretion

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11
Q

Describe the effects of PTH on bone.

A

Stimulates osteoclasts

Inhibits osteoblasts, this goes onto increase bone resorption.

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12
Q

Describe the effects of PTH on the small intestines.

A

PTH increases the activity of 1 alpha hydroxylase (in the kidneys), which is involved in the production of calcitriol, which increases calcium and phosphate absorption in the small intestine.

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13
Q

How does PTH increase calcium release from bone?

A

PTH has a direct effect in inhibiting osteoblasts. PTH makes the osteoblasts produce osteoclast activating factors (such as RANKL:Receptor activator of nuclear factor kappa-Β ligand) that bind to receptors on osteoclasts and stimulates the break down of bone matrix to release calcium.

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14
Q

What can stimulate PTH release?

A

Low plasma calcium concentration

Catecholamines (by binding to beta receptors)

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15
Q

Describe the negative feedback loops on PTH.

A

Increased plasma calcium concentration has a negative feedback effect on PTH
Calcitriol also has a negative feedback effect

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16
Q

What is the precursor of calcitriol?

A

Cholecalciferol

17
Q

Where does this precursor come from?

A

-Diet
-Sun Light (UV light converts 7-dehydrocholesterol to cholecalciferol)
NOTE: cholecalciferol is VITAMIN D3

18
Q

Describe the reactions that have to take place to convert the precursor to calcitriol.

A

Cholecalciferol travels to the liver where 25-hydroxylase converts it to 25-hydroxycalciferol, which is then stored in the liver.
It then moves to the kidneys where 1 alpha hydroxylase (stimlated by PTH) converts 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol (calcitriol)

19
Q

Describe the effects of calcitriol.

A

MAIN ACTION: stimulates calcium and phosphate absorption in the SMALL INTESTINE
Increased osteoblast activity on bone.
Kidneys - increases calcium and phosphate reabsorption

20
Q

How does calcitriol and PTH decrease phosphate reabsorption in the kidney?

A

They block the sodium/phosphate cotransporter

Calcitriol does this via the action of FGF23 (fibroblast growth factor 23)

21
Q

Describe the effects of calcitonin.

A

Calcitonin inhibits osteoclast activity
Calcitonin also affects the KIDNEYS - increase sodium excretion and hence increase urinary excretion of phosphate and calcium.
This decreases plasma calcium concentration

22
Q

State a physiological benefit of calcitonin.

A

During pregnancy women need a higher plasma calcium concentration (e.g. for milk), calcitonin protects the bone from break down.

23
Q

State three causes of hypocalcaemia.

A

Hypoparathyroidism: insufficient PTH
Pseudohypoparathyroidism: resistence to PTH
Vitamin D Deficiency

24
Q

What two signs are used to demonstrate hypocalcaemia?

A

Trousseau’s Sign: put slight pressure on the arm and the hand can go into contraction
Chvostek’s Sign : tap the facial nerve at the angle of the jaw you get muscles to contract
These are both signs of tetany

25
Q

What is pseudohypoparathyroidism and what are some clinical features?

A

Target organ resistance to PTH (also called Allbright Heriditary Osteodystrophy)
Round face, short, low IQ, short 4th metacarpal, hypothyroidism, hypogonadism

26
Q

What does vitamin D deficiency cause in children and adults and what are the clinical feature?

A

Children - rickets
Adults - osteomalacia

Bowing of bones in children
Fractures in adults

27
Q

State three causes of hypoparathyroidism

A
  • idiopathic
  • hympomagneseamia
  • supression by raised calcium concentration
28
Q

what are some diagnostic results in the different types of hypoparathyroidism

A

-in hypoparathyroidism you get an increase in plasma phosphate conc because PTH isn’t stimulating the excretion of phosphate from the kidneys. Decrease in plasma calcium and PTH
-pseudohypoparathyroidism- the parathyroid glands are producing insufficient PTH, but the target organs are resistent to PTH so plasma calcium conc is low and plasma phosphate and PTH increase
Vitamin D defiency: phosphate levels low, PTH normal and calcium low

29
Q

State three causes of hypercalcaemia.

A

Primary hyperparathyroidism
Tertiary hyperparathyroidism
Vitamin D Toxicosis

30
Q

Describe the differences between primary, secondary and tertiary hyperparathyroidism

A

Primary - caused by parathyroid adenoma producing huge amounts of PTH
Secondary - caused by other reasons e.g. renal excretion of Ca2+ ions leading to compensatory increase in release of PTH (this causes low Ca2+ because it is being lost from the kidneys)
Tertiary - initial chronic low plasma calcium concentration - parathyroid gland is massively stimulated for a long time and so PTH production becomes autonomous and stops responding to negative feedback (leads to hypercalcaemia in primary and teritary)

31
Q

State some consequences of parathyroid hormone excess.

A 
Kidney stones (calcium deposits) 
Increased risk of fracture
32
Q

What is a distinctive clinical feature of primary hyperparathyroidism?

A

Clubbing of the fingers

33
Q

Describe how calcium level are detected in the body?

A

It is detected by calcium sensing receptors which are found in the parathyroid gland and the renal tubules of the kidney.

34
Q

Describe how PTH is formed and how it goes on to effect?

A
  1. Initially synthesized as protein pre-proPTH
  2. PTH is a polypeptide of 84 amino acids
  3. Binds to transmembrane G-protein linked receptors
  4. Activation of adenyl cyclase, but also probably PLC as second messenger systems
35
Q

Describe how calcitonin is formed and how it goes on to effect?

A
  1. Synthesized as pre-procalcitonin
  2. Calcitonin is 32 amino acid polypeptide
  3. Binds to transmembrane G-protein linked receptor
  4. Activation of adenyl cyclase or PLC as second messenger systems

LCRS-Endocrinology (13 decks)

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